Cell biology of diabetic nephropathy: Roles of endothelial cells, tubulointerstitial cells and podocytes.
Cell biology of diabetic nephropathy: Roles of endothelial cells, tubulointerstitial cells and podocytes.
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DOI：
10.1111/jdi.12255
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发表时间：
2015-01
影响因子：
3.2
通讯作者：
Yokote K
中科院分区：
文献类型：
--
作者：
Maezawa Y;Takemoto M;Yokote K
糖尿病肾病是世界上发达国家和发展中国家终末期肾衰竭的主要原因。糖尿病影响肾的所有细胞类型，包括内皮细胞、小管间质细胞、足细胞和系膜细胞。在过去的十年中，足细胞损伤在糖尿病肾病的形成和发展中的重要性已经被确立和强调。然而，最近的研究结果为糖尿病肾病的发病机制提供了新的视角。当足细胞损伤开始时，肾小球内皮损伤已经存在于正常蛋白尿阶段。导致内皮损伤的小鼠基因靶向导致糖尿病肾病加速。小管间质损伤，以前被认为是肾小球蛋白渗漏的继发效应，现在被证明在糖尿病肾病的进展中具有主要意义。越来越多的证据表明，肾小球滤过屏障和小管间质室是一个复合的、动态的实体，任何一种细胞类型的损伤都会扩散到其他细胞类型，并导致整个器官的功能障碍。新知识的积累将有助于更好地了解糖尿病肾病的发病机制，并可能导致新的治疗策略的发展。
Diabetic nephropathy is the major cause of end-stage renal failure throughout the world in both developed and developing countries. Diabetes affects all cell types of the kidney, including endothelial cells, tubulointerstitial cells, podocytes and mesangial cells. During the past decade, the importance of podocyte injury in the formation and progression of diabetic nephropathy has been established and emphasized. However, recent findings provide additional perspectives on pathogenesis of diabetic nephropathy. Glomerular endothelial damage is already present in the normoalbuminuric stage of the disease when podocyte injury starts. Genetic targeting of mice that cause endothelial injury leads to accelerated diabetic nephropathy. Tubulointerstitial damage, previously considered to be a secondary effect of glomerular protein leakage, was shown to have a primary significance in the progression of diabetic nephropathy. Emerging evidence suggests that the glomerular filtration barrier and tubulointerstitial compartment is a composite, dynamic entity where any injury of one cell type spreads to other cell types, and leads to the dysfunction of the whole apparatus. Accumulation of novel knowledge would provide a better understanding of the pathogenesis of diabetic nephropathy, and might lead to a development of a new therapeutic strategy for the disease.
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DOI：
10.1152/ajpheart.00196.2002
发表时间：
2002-11-01
影响因子：
4.8
作者：
Brodsky, SV;Gao, SJ;Goligorsky, MS
通讯作者：
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影响因子：
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作者：
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